Download Ophthalmology Expert questions Evaluation of the red eye E H

Ophthalmology Expert questions
Evaluation of the red eye
EH
There are many conditions that can lead to a patient presenting with a red eye. A useful distinguishing feature is
whether the condition is painful or painless, and with further slit lamp examination for specific features.
Painless Red eye:
It is rare for a painless red eye to require urgent ophthalmological assessment. Conjunctival redness can be
diffuse or localized as follows:
Diffuse:
Lids Abnormal:
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Blepharitis – non specific generalized inflammation of the eyelids
o Treat with daily lid hygiene, lubrication as required and non-urgent referral
Ectropion – lids turning outward with exposure of conjunctival sac
o Topical lubrication with non-urgent referral
Trichiasis
o Epilate, lubricate with non-urgent referral
Entropion – lids turning inwards with eyelids abrading cornea

o Check cornea with fluorescein
o Intact cornea – lubrication with non-urgent referral
o Epithelial defect – tape back eyelid from the cornea and manage as corneal foreign body
Eyelid lesion
o no overt infection/inflammation and no ocular involvement – non-urgent referral, consider
topical antibiotics
Lids Normal

Conjunctivitis – most cases are painful
Localised
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Pterygium – raised yellowish fleshy lesion at limbus, may become painful and red if inflamed
o Lubrication and sunglasses
o Non-urgent referral
Corneal foreign body
o Remove foreign body and treat with topical antibiotics
Ocular trauma
o Treatment as for blunt or penetrating trauma
o Topical antibiotics for superficial trama
Subconjunctival hemorrhage –
o blood redness, unilateral, localized and sharply circumscribed
o Underlying sclera not visible
o No inflammation, pain or discharge
o h/o minor injuries, coughing, sneezing
o common with antiplatelet agents and anticoagulants
 check manage BP
 if on warfarin- check INR
 use lubricating eyedrops
 refer if worsens or pain develops
Painful Red Eye
Cornea Abnormal
Use fluorescein to ascertain nature of any epithelial defect
 Herpes simplex infection
o Dendritic ulcer
o Treatment with topical acyclovir
o Urgent ophalmologist review within 24 hrs
 Bacterial ulcer
o Often h/o contact lens use
o
o


Epithelial defect with opacified base
Immediate consult by phone, may require admission for microbial investigation and antibiotic
treatment
Marginal ulcer
o Secondary to blepharitis
o Ulcer at corneal periphery
o Immediate consult by phone and urgent referral
Foreign body/ corneal abrasion
o Remove foreign body treat with topical antibiotics
o Treatment for corneal abrasion
Eyelid Abnormal
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Chalazion, stye
o Localized eyelid inflammation with minimal ocular involvement
o Treat with antibiotic ointment if indicated
o If acutely inflamed treat with oral antibiotics and warm compresses
o Non-urgent referral
Acute blepharitis
o Localized eyelid inflammation with minimal ocular involvement
o Treat with antibiotic ointment is indicated
o Non-urgent referral
Herpes Zoster
o Vesicular rash
o Treat with oral antivirals within 72 hrs of appearance of rash
o Non-urgent referral – if cornea normal
Diffuse conjunctival injection
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Viral conjunctivitis
o Contact history
o Burning sensation and watery discharge – not purulent
o Highly contagious – standard precautions
 Wash hands and separate tissues to avoid infection of other eye
 Cool compresses
 Lubricants
 Antibiotic drops if indicated
 Never steroids!
 Photphobia or marked decrease in visual acuity – urgent referral
Allergic conjunctivitis
o Itch!!!
o Atopic history: asthma, eczema, conjunctivitis
o Cool compresses, ocular lubricant
o Semi-urgent referral – within 3 days if symptoms not controlled
Bacterial conjunctivitis
o Tender inflamed conjunctiva with purulent discharge – often bilateral
o No corneal or anterior chamber involvement
o Systemically well – common in children and elderly
 Regular hygiene
 Wash hands and separate tissues
 Topical antibiotics QID for 5 days
o Refer if vision affected, symptoms not improving or persists without improvement in 5days
Dry eyes
o Chronic ocular condition
o Symptoms worsen in the evening
 Lubricants

Non-urgent referral
Acute angle closure glaucoma
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Cornea usually has hazy appearance
Anterior chamber shallow with irregular semidilated pupil
Affected eye very tender and tense to palpation
Systemic symptoms of headache, nausea and vomiting
o Urgent referral and immediate consult
Ciliary injection/ Scleral involvement

Scleritis
o Vision may be impaired
o Sclera thickened and discoloured
o Associated h/o vasculitis or connective tissue disease to be sought
o Urgent referral – within 24 hrs
Anterior chamber involvement
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Acute anterior uveitis (Iritis)
o Pain, photophobia and red eye
o Anterior chamber cloudy from cells and flare
o Urgent referral < 24 hrs.
Hypopyon
o Visible accumulation of white cells inferiorly seen in severe uveitis
o Urgent referral + consult by phone – to investigate infection, inflammation or ocular
malignancy
Hyphaema
o Usually trauma related but consider non accidental injury in children and blood dyscrasias
o Bed rest
o Urgent referral <24hrs
Evaluation of the painful eye
EH
Painful eye is one of the common presentations to emergency department and though most causes may be
managed well, some serious disorders need urgent evaluation and early recognition and management.
Eye pain can be broadly divided into ocular pain and orbital pain.
Ocular pain: pain arising from the anterior structures of the eye i.e. cornes, anterior chamber, iris and may be
described as sharp, aching, burning or foreign body sensation.
Orbital pain: a more dull aching deep seated pain originating from the posterior and retrobulbar structures of the
eye.
Both types of pain may co-exist and the type of pain is not sensitive enough to suggest a diagnosis and all
patients need to undergo a detailed ophthalmologic and sometimes physical examination to rule out serious
disorders.
The most common causes overall are
 Corneal abrasion
 Foreign bodies
However, most corneal disorders can cause eye pain. A feeling of scratchiness or of a foreign body may be
caused by either a conjunctival or a corneal disorder.
Cause
Suggestive findings
Disorders affecting the cornea
Contact lens keratitis
h/o contact lens use, ocular
pain, bilateral red eyes,
lacrimation and corneal
edema
Corneal foreign body or
h/o injury, unilateral pain
abrasion
on blinking, FB sensation
lesion/FB visible on
fluorescein examination
Diagnostic approach
Treatment
Clinical evaluation
Urgent referral
Clinical evaluation incl.
Eyelid eversion
Corneal ulcer
Scrapings may be needed
for cultures done by
opthal.
Clinical evaluation and
viral swabs
Topical antibiotics and
cycloplegic agent,
analgesia
Removal of foreign
body
Urgent referral, topical
acyclovir or antibiotics
depends on cause
Urgent referral
Symptomatic
management,
preventive measures
and analgesia
Epidemic
keratoconjunctivitis
Herpes zoster
ophthalmicus
Herpes simplex keratitis
Flash burns
Symptoms as in FB. Ulcer
visible on fluorescein
examination
Gittiness, bilateral red eys,
often eyelid edema,
copious discharge,
preauricular
lymphadenopathy,
chemosis, occasionally
severe temporary loss of
vision. Punctuate staining
on fluorescein
Unilateral vesicles and
crusts in typical
dermatome distribution,
eyelid edema, severe pain
delayed, associated with
uveitis
Onset after conjunctivitis
with blisters on eyelids
Classic dendritic lesion on
fluorescein
Onset after exposure to
excessive UV light e.g.
welding, bright sun on
snow, bilateral with
marked injection,
Clinical diagnosis, viral
cultures if unclear
Oral retrovirals within
72 hrs of rash
Non urgent referral
unless corneal
involvement
Clinical diagnosis, viral
cultures if unclear
Topical acyclovir,
urgent referral
Clinical evaluation
Topical antibiotic QID
and cyclopegic for
comfort, oral analgesia
PRN
punctuate staining on
fluorescein
Other Ocular disorders – most cause orbital pain as well
Acute angle-closure
Severe ocular/ orbital pain,
glaucoma
systemic symptoms, halos
around light, hazy cornea.
Marked erythema, raised
IOP
Anterior uveitis
Ocular pain, ciliary flush,
photophobia. H/o systemic
disorder. Cells and flare on
slit lamp, rarely hypopyon
Endophthalmitis
Severe orbital pain and
decreased visual acuity,
intense conj. Hyperaemia.
H/o recent surgery. Cells
and flare
Optic neuritis
Mild pain may worsen
with eye movement, vision
loss(blind spot), afferent
pupillary defect, swollen
optic disk
Orbital cellulitis
Orbital pain, periorbital
pain, unilateral propotosis,
impaired eye movements,
periorbital edema,
systemic findings
Orbital pseudotumor
Pain. Limited movements,
propotosis and congestion.
h/o systemic disorder
Scleritis
Very severe pain,
photophobia, lacrimation,
discoloured patches under
bulbar conjunctiva, sclera
edema. h/o AI disease
Disorders causing referred pain
Cluster headache
Prior history, ass
headaches, rhinorrhea,
flushing, lacrimation,
photophobia
Sinusitis
Periorbital edema nil other
ocular signs unless orbital
contents involved
s/o sinusitis
Clinical and by tonometry
Clinical evaluation
Topical β-blocker,
topical α-agonist,
azetazolamide,
mannitol, pilocarpine
(mydriatic). Urgent
referral
Topical steroids by
ophth. Treat
underlying cause
Clinical evaluation,
cultures by ophth.
Sedation, analgesics,
subconjunctival and IV
antibiotics guided by
cultures
Ophthalmoscopy, MRI
Urgent referral,
systemic steroids if
demyelinating lesions
Clinical evaluation, CT or
MRI
Urgent referral,
admission, IV
antibiotics
Difficult, early referral, CT
or MRI
Trial of systemic
steroids
Clinical evaluation
Treatment for
underlying cause
NSAID and/or steroids
Clinical evaluation, eye
exam may be difficult
Treat underlying cause
Clinical evaluation, +/- CT
Management of
sinusitis
Key Points
 Most diagnoses can be made by clinical evaluation.
 Infection precautions should be maintained when examining patients with bilateral red eyes.
 Important danger signs are vomiting, halos around lights, fever, decreased visual acuity, proptosis, and
impaired extraocular motility.
 Pain in the affected eye in response to shining light in the unaffected eye when the affected eye is shut
(true photophobia) suggests a corneal lesion or uveitis.
 If pain resolves with a topical anesthetic (eg, proparacaine) cause of pain is a corneal lesion.
 Hammering or drilling on metal is a risk factor for occult intraocular foreign body.
Sudden visual loss
EH
All presentations of sudden persistent loss of vision require an urgent ophthalmology
consult.
Transient Ischemic attack – Amaurosis Fugax
 Monocular viasul loss usually lasts seconds to minutes, may last 1-2 hrs. vision returns to normal
 Essentially normal fundus exam, sometimes embolus seen
 Other neurological signs associated with TIA
 Investigate as for TIA
 Management as for TIA
Central retinal vein occlusion
 Sudden painless loss of vision
 Risk factors – age, HT and DM
 Visual acuity changes depending on severity and duration of illness
 Fundus – large areas of hemorrhage
 Screen for DM/HT and manage same
 Urgent referral to Ophthalmologist
Central retinal artery occlusion
 Sudden painless loss of vision
 Visual acuity< 6/60
 Relative afferent papillary defect marked
 Fundus – pale arteriolar and venular narrowing, abnormal red reflex
 Urgent ESR/CRP to rule out arteritis
 Urgent referral to ophthalmologist
 Management as for TIA
Optic neuritis
 Painless loss of vision over hours to days
 Varying degress of visual loss
 Reduced visual acuity, colour and contrast vision
 Usually unilateral but may be bilateral
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Females 18-45 most commonly
Signs:
o RAPD
o Decreased colour vision
o Patchy visual field defects
o Swollen optic disc
o Other focal neurologic signs
 Urgent referral to ophthalmologist and neurologist for urgent MRI and
 Need for systemic steroids
Giant cell arteritis
 Typically age >50 years
 Raised ESR and CRP
 Symptoms
o Temporal headache
o Scalp tenderness
o Jaw claudication
o Fever and night sweats
o Muscle pain and weakness
 Signs
o RAPD
o Poor visual cuity
o Papable, tender nin-pulsatile temporal artery
o Swollen optic disc
 Management:
o Urgent markers – ESR/CRP
o Urgent referral ophthalmologist/ neurologist
o Temporal artery biopsy to confirm diagnosis
o Oral steroids
Retinal detachment
 Separation of sensory retina from retinal pigment epithelium commonly due to predisposing retinal
defect
 Painless loss of vision, recent h/o increased visual floaters/flashes; dark shadow in vision of affected
eye
 h/o myopia and previous trauma increases risk
 signs
o reduced visual acuity
o abnormal red reflex
o detached retina may be seen
 management:
o bed rest
o urgent ophthalmology consult
o surgery
Foreign bodies
 Conjunctival
 Corneal
DIS H
DIS H
One of the commonest eye related presentation to the emergency department. Though most case may be
managed expediently, the condition is associated with significant patient discomfort and morbidity if not
properly managed.
Any foreign body penetration of the cornea or retained foreign body will require urgent referral to
ophthalmologist - immediate consult by phone.
History:
 Type of foreign body: organic vs. inorganic material
o Organic material may lead to infection
o Metallic FB – rust rings with persistent inflammation and epithelial defect
 Velocity of impact
o High speed motor drilling without eye protection – penetrating corneal/ sclera injury
Examination
 Visual acuity
 Slit lamp
o Size, site, nature of FB and depth of penetration
 Examine cornea, AC, iris, pupil and lens for any distortion – evidence for penetrating ocular trauma
 Evert eyelids to exclude retained FB
Treatment/ investigation
 Topical anesthesia
 Foreign body removal under slit lamp
 Rust ring removal by ophthalmologist or experienced ED physician
 Fluorescein to assess epithelial defect
 Topical antibiotic (qid) and cycloplegic for comfort
 No need for continued topical anesthetic
 If central corneal FB – epeithelial defect to be closely followed up with ophthalmologist
 Patient to avoid contact lens use for at least a week or resolution.
Reasons for urgent referral < 24 hrs.
 FB not completely removed
 Underlying opaque defect s/o abscess
 Persistent epithelial defect after 3 days
Ocular burns
 Caustic
 Flash burns
 Thermal
DIS H
DIS H
DIS H
Always have high degree of suspicion in case of children presenting with ocular burns for un-explained
Non-accidental injury(NAI)
Chemical Burns
History
 Time since injury, mechanism of injury
 Check in patients with facial injuries
 Type of chemical – acid or alkali
o Alkali more harmful – lime, mortar, plaster, drain cleaner or ammonia etc.
o Acids – toilet cleaner, car battery fluid, pool cleaner etc.
 First aid at scene and on transit
Examination
 Topical anesthesia and systemic analgesia if indicated
 Management of concurrent injuries
 Assess degress of vascular blanching particularly at limbus → proportional to severity of burn
Treatment
 Eye irrigation for chemical burns –
o Check pH optimum 6.5 – 8.5 acceptable, goal neutral pH 7.4
o Commence iriigation with 1L of neutral solution e.g. NS, Hartmanns
o Evert eyelid – clear debris
o Use Morgan lens if available
o Review after 1L irrigation – wait 5 mins before rechecking pH
o Recommence irrigation if target pH not reached
o May need at least 30 minutes in case of severe burns
 Test and record visual acuity
 Contact poisons information or chemical manufacturer for any further information
 Topical antibiotic drops, cycloplegics and mydriatics.
 Urgent ophthalmology consult and review if any visual acuity loss or corneal opacification
Complications
 Acid quickly precipitates the superficial tissue proteins of the eye, producing the typical "ground glass"
appearance of the cornea. Penetration is limited by local buffering and barrier effects of the precipitated
proteins. Damage sustained secondary to acid burns in most cases is immediate and limited to the area
of contact. The posterior segment of the eye rarely suffers injury, and there are usually no late effects
such as cell disruption or tissue softening.
 Alkali burns are more severe, and results are frequently unsightly and disastrous. In general, the higher
the pH of the alkali, the more damage. In a short period, strong alkali can penetrate the cornea, anterior
chamber, and the retina, with destruction of all sensory elements, thus causing complete blindness.
 Severe chemosis, blanched conjunctiva, and an opacified cornea obscuring view of the iris or lens may
occur.
 The penetration of alkali can continue for hours to days, resulting in globe perforation.
 The conjunctiva, and scleral blood vessels and collecting veins of the anterior chamber may be
destroyed, leading to secondary glaucoma.
 Chronic inflammation of the iris and ciliary body (iridocyclitis) and adhesions between lens and iris
(posterior synechiae) are possible complications of ocular burns.
 Other complications of eye burns include ectropion (lid deformity), cataract formation, scarring and
marked revascularization of the cornea, and

scarring of both palpebral and bulbar conjunctiva with resulting adhesions between the lids and globe
(symblepharon).
Thermal burns
Clinical Findings
 Injury due to thermal burns of the eyelids, cornea, and conjunctiva may range from minimal to
extensive. Superficial corneal burns have a good prognosis, though corneal ulcers may occur as a result
of loss of corneal epithelium.
 Thermal burns of the skin of the eyelids may be first, second, or third degree.
 Conjunctival hyperemia is noted.
 The cornea may show diffuse necrosis of the exposed corneal epithelium in the interpalpebral area.
 Corneal haze due to corneal edema is frequently seen in thermal burns of the cornea and may lead to
decrease in vision.
Treatment
 Provides systemic analgesia
 Mydriatic agent instillation and
 Urgent ophthalmological consult
Flash burns
History
 Electric arc welding or sun lamp without eye protection
 Extreme sunlight exposure especially in snow
 Symptoms typically occur within several hours
 Intense pain, red eyes usually bilaterally, blepharospasm and tearing
Examination
 Topical anesthesia both therapeutic and for ease of examination
 Check visual acuity
 Slit lamp – widespread superficial epithelial defect staining with fluorescein
Treatment
 Topical antibiotic QID and cycloplegic e.g. Homatropine 2% BD for comfort for three days
 To represent if symptoms have not appreciably improved after 24 hours
Follow
 If required – non-urgent within 3 days.
Glaucoma
DIS H
Glaucoma is an acquired chronic optic neuropathy characterized by optic disk cupping and visual field loss. It is
usually associated with elevated intraocular pressure.
Etiology
 Primary glaucoma
o Open angle
 Primary open angle
 Normal tension
o Angle closure
 Acute
 Subacute
 Chronic
 Congenital glaucoma
 Secondary glaucoma
o Pigmentary
o Exfoliation
o Lens changes
 Dislocation
 Advanced cataract phacolytic
o Uveal tract changes
 Uveitis
 Posterior synechiae
 Tumor
 Ciliary body swelling
o Trauma
 Hyphema
 Angle contusion
 Peripheral anterior synechiae
o Post operative
o Neovascular
 DM
 Central retinal vein occlusion
 IO tumor
o Iatrogenic – steroid induced
 Absolute glaucoma – end point of all types – hard sightless, often painful eye.
Pathophysiology
The mechanism of raised intraocular pressure in glaucoma is impaired outflow of aqueous resulting from
abnormalities within the drainage system of the anterior chamber angle (open-angle glaucoma) or impaired
access of aqueous to the drainage system (angle-closure glaucoma).
Treatment is directed toward reducing the intraocular pressure and, when possible, correcting the underlying
cause. Although in normal-tension glaucoma intraocular pressure is within the normal range, reduction of
intraocular pressure may still be beneficial.
The most significant type of glaucoma presenting to ED, with significant morbidity outcomes is Acute AngleClosure Glaucoma.
Acute Angle-Closure Glaucoma
Primary acute angle-closure glaucoma occurs in eyes with narrow anterior chamber angles, such as in the older
age groups, hyperopes, Inuits, and Asians
Etiology
May be precipitated by
– Pupillary dilation from sitting in the dark
– Stress
– Pharmacologic mydriasis for ophthalmologic examination (rarely)
– Medications with anticholinergic or sympathomimetic activity
Secondary acute angle-closure glaucoma may occur in uveitis
Clinical findings
 Extreme ocular pain
 Blurred vision, typically with halos around lights
 Nausea and vomiting
 Red eye, cloudy cornea, usually with a moderately dilated, non-reactive pupil
 Intraocular pressure usually over 50 mm Hg, producing a hard eye on palpation
Diagnosis
 Markedly elevated intraocular pressure with shallow anterior chamber in both eys
 Must be differentiated from conjunctivitis, acute uveitis and other corneal disorders
Treatment
 Immediate referral and early consultation with ophthalmologist with early review
 500mg IV acetazolamide, followed by 250mg orally QID
 If no response, consider 1-2 g/kg of osmotic diuretic e.g. IV mannitol or urea
 After IO pressure is reduced, topical 4% pilocarpine, 1 drop every 15 min for 1 hour, then QID – used
to reverse angle closure
 Topical β-blocker timolol 0.5% one drop and topical α-agonist Iopidine 0.1% one drop
 Topical steroids after ophthalmology consult
 Definitive treatment is generally laser or surgical peripheral iridotomy usually done bilaterally.
Ocular trauma
Lid Laceration
Any laceration other than superficial skin that involves the lid margin will need ophthalmological referral.
(Check for tetanus immunisation status). An eyelid laceration is a potential penetrating eye injury until
proven otherwise.
History
Four basic questions are:
 which eye is injured?
 how did it happen?
 when did it happen?
 what are the symptoms?
Nature of injury – was there any possibility of penetration into the lid/orbit?
Examination
Wound examination – size and depth.
 All wounds should be explored fully for extent of damage.
 Visual acuity.
 Superficial ocular examination with magnification to assess for any corneal/conjunctival laceration or
penetration.
 Further ocular examination including dilated fundus examination as determined by history and
examination findings.
Treatment/Investigation
 Orbital X-Ray or CT if indicated for foreign bodies or orbital fracture.
If superficial laceration:
 Clean the area and surrounding skin with antiseptic such as Betadine.
 Subcutaneous anaesthetic with vasoconstrictor (2% Lignocaine with Adrenaline).
 Irrigate and debride the wound thoroughly with saline.
 Identify foreign bodies if applicable.
 Suture with a 6/0 non-absorbable suture.
When to refer?
Referral to an ophthalmologist:
 If the eyelid laceration is associated with ocular trauma requiring surgery such as ruptured globe or
intraorbital foreign body.
 If the laceration position is nasal to either the upper or the lower eyelid punctum, for the possibility of
damage to the nasolacrimal drainage system.
 If there is extensive tissue loss or distortion of the anatomy.
 If there is full thickness laceration or the laceration involves the lid margin.
Broad spectrum antibiotic cover if there is significant risk of contamination, or debridement of necrotic tissue.
Blunt Ocular trauma
Blunt trauma to the eye may result in considerable damage to the intraocular contents. Fracture of the orbital
wall may occur due to the transfer of mechanical energy to relatively thin orbital bone.
Ruptured globe
Trauma of sufficient force may result in globe rupture and typically occurs in the areas where the scleral wall is
thinnest:
 at the limbus (which would be visible via the slit lamp) or
 Behind the insertion of the rectus muscle (which would result in reduced ocular motility, loss of red
reflex and vitreous bleed).
Examination
 Visual acuity.
 Ocular movements – if there is considerable eyelid oedema, carefully lift up the lid while viewing the
eye to ensure there is no obvious rupture.
 Reduced movement may suggest ruptured globe or orbital wall fracture.
 Slit lamp – looking for evidence of rupture (often at the limbus). Examine for blood in the anterior
chamber.
 Examine the eyelid for lacerations.
 Ophthalmoscopy – Red reflex (missing in intraocular haemorrhage or retinal detachment). Look for
any retinal pathology (after dilating the pupil).
Investigations

CT scan (axial and coronal) for orbital wall fracture if indicated
Follow up - When to refer?
 Non-urgent referral within 3 days if the above findings are negative.
 Urgent referral to ophthalmologist - immediate consult by phone if findings are suggestive of
intraocular haemorrhage, ruptured globe or orbital wall fracture
Treatment

Topical antibiotic drops for superficial trauma
Penetrating Ocular trauma
All penetrating trauma require urgent referral to ophthalmologist - immediate consult by phone
following appropriate pre-op workup.
History
 Mechanism of trauma – any history suggestive of a penetrating trauma.
 The type of projectile and the likely velocity (e.g. low or high) should be documented.
 Small projectiles at high velocities increase the likelihood of penetrating trauma. Symptoms
include loss of vision, pain on movement and diplopia.
 Was the patient wearing eye protection?
 Any previous history of ocular trauma or previous surgery is to be documented and may suggest
reduced integrity of the wall of the globe.
Examination
Examination may only need to be cursory if the trauma is obvious otherwise: –
 Visual acuity.
 Direct ophthalmoscopy – loss of red reflex may suggest retinal trauma or detachment.
 Slit lamp – looking for distorted anterior chamber structures or corneal/scleral breaks.
Treatment
 Ensure nil by mouth status. Strict bed rest. Injectable analgesia/antiemetic if required.
 CT scan of the orbit to exclude retained ocular/orbital foreign body after discussion with
ophthalmologist.
 Shield (not pad) the eye making sure not to increase the intraocular pressure with further loss of ocular
contents.
 No ointment for penetrating eye injury.
 Check for tetanus immunisation status as per current protocol.
 Commence broad spectrum IV antibiotics.
Orbital Cellulitis
 Orbital
 Pre-orbital
DIS H
DIS H
Cellulitis as previously defined may involve the tissues anterior to the orbital septum (periorbital cellulitis) or
within the orbit (orbital cellulitis).
Characteristic
Age
Organisms
Pathophysiology
Clinical features
 Periorbital
swelling
 Proptosis
 Extraocular eye
movements
 Fever
Investigations
CT scanning
Complications
Treatment
Orbital cellulitis
Children less than age 3
S. Aureus, S. Pneumoniae, H.
Influenzae (less due to universal
immunisation)
Hematogenous seeding or direct
extension from ethmoid sinus
Periorbital cellulitis
Any age
S. Aureus
Present, more prominent
Present
Present
Restricted
Absent
Normal
Contiguous spread most common
Usually present
Usually absent
WCC, cultures may be +/-
Indicated if any eye movement
disability – positive for collection/
soft tissue swelling
Subperiosteal abscess, threatens
integrity of eye. Intracranial
extension rare
IV antibiotic therapy directed
against S.aureus, pneumococcus
and H.influenzae
Ceftriaxone/dicloxacillin
Urgent referral to ophthalmology
Leucocytosis and blood cultures
usually positive
Lumbar puncture indicated if
systemically unwell
Not indicated
Retro-orbital changes usually
absent
May serve as focus for metastatic
bacterial disease, particularly
meningitis
Same as orbital cellulitis
Semi-urgent ophthalmology
referral